In this segment we are going to deal with coronary artery disease,
the commonest cardiovascular disease in the world.
As you can see from this slide, there are millions of people affected by coronary artery disease
in North America, in Western Europe, in Asia, and even in Latin America and in Africa.
This disease has now become the number one cause of death in the world.
It is the result of the atherosclerotic process and we've talked about this a number of times in earlier lectures.
What happens is there is an injury to the endothelium which is the skin like lining on the inside of a blood vessel.
Once that happens, then lipids, i.e. cholesterol or low density lipoprotein cholesterol,
are able to gain access into the area under the endothelium.
They set off an inflammatory reaction which feeds upon itself and gets gradually worse
so that more LDL cholesterol gets in through the endothelium, setting off more information
and eventually, you have collections of cholesterol, scar tissue and inflammation cells
that represent the atherosclerotic process.
And in this little cartoon, you see a little diagram showing the various inflammatory cells
working their way into the area under the endothelium that is under the little skin of the artery.
Now, what happens is, as time goes along these atherosclerotic deposits which contain calcification,
they contain cholesterol deposits, they contain fibrous tissue which is scar tissue,
they contain inflammatory cells and eventually they can markedly narrow the channel.
And here you see a little diagram, actually, I use to train individuals to do the angioplasty,
the balloon opening and you can see on the left hand side, the severe atherosclerotic narrowing.
You can see the collapsed balloon being slid through the narrowing,
then the balloon in inflated and it opens up the channel again in the far right diagram.
This is getting a little ahead of ourselves, but I wanted you to understand already
that coronary artery disease is in a sense a plumbing problem.
The plumbing has become inflamed and narrowed by the biological process
and what we do as interventional cardiologist, is try and reopen those arteries as well as we can.
So let me review once more then what I just said with a few cartoons.
You can see on the left hand side that there's been a little tear,
a little injury to the endothelium, the skin on the inside of an artery.
Now this injury can be from a variety of sources, it can be from high blood pressure,
it can be from a very toxic level of high cholesterol, it can be from substances
and cigarette smoke, it can be from the diabetic condition,
a number of things can injure the endothelium.
What happens is once there's a little tear, you can see these little white balls, those are platelets,
the little clotting factors that cover over the tear but that having happened,
that's an area that allows cholesterol to get in under the surface
and here you see from an actual autopsy specimen, quite a collection
below the lumen or the opening of the artery and all of that material in there consist
of cholesterol and scar tissue and inflammatory cells.
You can see, you've seen this diagram before, actually the channel,
which is the black area, is still quite open and so decent blood flow
is going down this artery even though there's already fairly far advanced atherosclerosis.
Unfortunately, what often happens is, the skin covering that collection of lipid and scar tissue,
can break and it can break because of a sudden episode of high blood pressure
or it can break because the inflammatory cells dissolve some of the material
that's holding the cholesterol and fibrous tissue in
and what happens then is you can activate actually a blood clot forming there
that eventually can completely block the artery and lead to no blood flow,
no nourishment going down the artery and that is a myocardial infarction or death of heart cells.
In this slide, you can see already on the left hand side that here is small tear developing in the atherosclerotic lesion.
The white area here is the open artery, the open lumen or channel of the artery
and you can already see that there's a break about to occur in this artery,
and when that breaks occur, suddenly, the flowing blood sees all the material
that's underneath that break and a blood clot rapidly forms and here you see an example.
Actually, the endothelial layer of the heart blood vessel has been pulled away
and actually lead to a clot that completely blocks the artery.
When the artery is blocked again, remember what happens,
downstream there's no nourishing blood and heart cells begin to die, that's a myocardial infarction.
Infarction means death of tissue, myocardium, of course is heart muscle
and myocardial infarction is due to death of heart tissue because of lack of nourishing blood.
Now, what are the differences between angina, which many patients with atherosclerosis have,
and a myocardial infarction? Well, you'll see here listed on this slide,
all of the differences between these two.
Let's think about it for a moment, when a patient has narrowing in the blood vessels
and suddenly they increase their activity so that their heart rate and blood pressure goes up,
what happens is there's a marked increase in the demand for oxygen and nutrients by the heart cells
because they're working harder of course.
If there's a narrowing in the artery, then that demand for more blood flow,
more nourishment cannot be met, so there's, if you will, a deficit in nourishing blood and oxygen
reaching the myocardial cells and a signal is sent to the central nervous system
which is perceived as discomfort and we talked about this before,
remember in an example way back when I talked about a patient, a Mr. AB, who had angina.
The symptom comes on when the patient exerts themselves and then goes away when they sit quietly, why?
Because the blood pressure and the heart rate go down,
there's not so much demand for increased oxygen and nutrients,
and the patient feels better because the symptom resolves.
I often explained it to patients, it's like you've got a block in the fuel line from your gas tank to your motor.
When you go uphill and you step on the gas to try and increase the amount of gas going in to the motor,
it doesn't happen because there's a block in the fuel line, a narrowing in the fuel line
and the motor sputters, that sputtering is angina pectoris,
but when the car reaches the top of the hill and slides down the other side,
you take your foot off the gas, the sputtering goes away and the motor runs fine
because you're not asking the motor to do quite so much.
Myocardial infarction is a different story.
It's not a problem with supply and demand,
it's a problem with supply, there's a sudden cut off of the blood flow into the coronary artery bed
and suddenly heart cells begin to die because of lack of nourishment.
The pain, does not go away with rest, in fact it often increases, starts quiet
and builds and the patients may have associated symptoms.
They may become short of breath, they begin to sweat
because the nervous system is activated, they become anxious.
It's very different from angina pectoris which is noticed when the patient
let's say walks up a hill or a flight of stairs, they rest and the symptom goes away.
But with myocardial infarction or a heart attack, the pain doesn't go away
and it's associated with a whole lot of systemic symptoms and of course it's a medical emergency.
Again, just to remind you, an angina it's an imbalance between supply and demand.
Normally, in the heart, whenever we increase our workload, the coronary arteries dilate,
they increase the blood flow to the myocardial cells
just like increase gas through an open fuel line and everything goes fine.
When there's an imbalance in the situation, then suddenly,
there's a lack of nourishment and the heart signals through the brain,
oh, there's discomfort here because I'm having a lack of oxygen and blood
for the increased work that I'm doing.
Rest, the imbalanced disappears and the symptom disappears.